Our major objective is to relate lung injury to its utilization of substrates. We will relate the availability of glucose to the isolated perfused lung to its tolerance for ischemia. We also plan to determine some aspects of the mechanisms by which the isolated perfused lung has increased glucose consumption when it is distended. This effect may be related to the pulmonary edema which develops in distended lungs or to the effects of distension. We also will ventilate rabbits and dogs with pressures which produce pulmonary edema or air embolism in the rat. These studies may increase or decrease our concern that similar effects occur in humans.